Mouse pMAPT /pTAU(phosphorylated microtubule-associated protein tau) ELISA Kit (E-EL-M1289)

This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Mouse pMAPT/pTAU. Standards or samples are added to the micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for Mouse pMAPT/pTAU and Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Mouse pMAPT/pTAU, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm ± 2 nm. The OD value is proportional to the concentration of Mouse pMAPT/pTAU. You can calculate the concentration of Mouse pMAPT/pTAU in the samples by comparing the OD of the samples to the standard curve.

Vascular endothelial growth factor A (VEGF-A) is the founding member of the VEGF family within the platelet-derived growth factor (PDGF) supergene family. It functions as a disulfide-linked homodimer, and alternative splicing generates several isoforms differing in heparin binding and matrix diffusion. VEGF-A is strongly induced by hypoxia through hypoxia-inducible factor 1alpha (HIF-1alpha) and by cytokines including IL-1 and IL-6, and it is a key regulator of angiogenesis during development and adult life. Binding VEGF receptor 1 (VEGFR-1) and especially VEGFR-2 activates receptor tyrosine kinase signalling that promotes endothelial proliferation, survival, migration and tube formation and increases vascular permeability. VEGF-A drives embryonic vascular network formation and, after birth, supports endothelial maintenance, tissue repair, wound healing and collateral vessel formation in ischaemia, functioning as the principal effector of the hypoxia response and of physiological and pathological neovascularisation. VEGF-A levels therefore reflect angiogenic activity, and elevated concentrations accompany tumour growth, ocular neovascularisation, inflammatory disease and ischaemic disorders. Quantitative measurement supports angiogenesis, tumour and ischaemia research as well as monitoring of hypoxia- or drug-induced production and of pro- and anti-angiogenic interventions. As the principal target of anti-angiogenic therapy, including neutralising antibodies and tyrosine kinase inhibitors, VEGF-A is measured to characterise treatment response and resistance.